Fearful 'superbugs' may be cured by ordinary painkillers

Anti-inflammatory painkillers found to have secondary effect of preventing multiplication of bacteria

"Superbugs,"
diseases which seem immune to the most advanced reaches of science, may
in fact be vanquished with something you may have in your drug cabinet
right now. In a study published in the scientific journal "Chemistry
& Biology," Australian researchers have found that many common
painkillers have the secondary effect of preventing some bacteria from
multiplying.

Bromfenac is a pain-killing medication usually applied to the eyes following cataract surgery.

Highlights

LOS ANGELES, CA (Catholic Online) - Researchers at the University of Wollongong in Australia found this to be true of anti-inflammatory painkillers, which are used for maladies such as arthritis and eye ailments.

Drug-resistant infections have been blamed on the excessive use of antibiotics, resulting in the reduced effectiveness of many traditional drugs. Once easily killed by antibiotics, the now resilient bacteria have sent shockwaves throughout the medical community. WISH POPE FRANCIS A HAPPY ANNIVERSARY!

Infections caused by drug-resistant bacteria hit about two million people in the U.S. each year, leading to at least 23,000 deaths, according to data from the U.S. Centers for Disease Control and Prevention.

Drugs involved in the Australian study are non-steroid anti-inflammatory drugs, a class of medications that also includes such common household over-the-counter medication such as aspirin and Ibuprofen.

"The fact that the bacteria-killing effect of the anti-inflammatory drugs is different from conventional drugs means that the NSAIDS could be developed into new kinds of antibiotics that are effective against so-called superbugs," the research report's lead author, Associate Professor Aaron Oakley, said. "This is important because the superbugs have become resistant to many, and in some cases most of the available antibiotics."

Three pain relievers used to treat various ailments in people as well as pets bromfenac, carprofen and vedaprofen - and found that they all had the ability to stop replication among some bacteria.

The researchers said they found that the drugs acted on bacteria in a way that is fundamentally different from current antibiotics by binding to a part of a bacterium called a "DNA clamp," preventing the organism from replicating or repairing its DNA and thus eventually killing it. No current antibiotics target the DNA clamp, Oakley says.

Some experts said it is too early to know if the study's findings will lead to a new class of antibacterial drugs. "I saw no compelling connection made between the biochemical activities that were observed and the antibacterial activity," Richard H. Ebright, professor of chemistry and chemical biology at Rutgers University, says.

It's agreed that the Australian research is headed in the right direction. "While our research is a long way from clinical trials, the fact that the bacteria-killing effects of the anti-inflammatories are different from conventional drugs means that they could be developed into new kinds of antibiotics," Ebright said.